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Is Tranexamic Acid Associated With Mortality or Multiple Organ Failure Following Severe Injury?

Richards, Justin E.∗,†,‡; Fedeles, Benjamin T.; Chow, Jonathan H.; Morrison, Jonathan J.†,‡; Renner, Corinne; Trinh, Anthony T.; Schlee, Caroline S.; Koerner, Ken∗,†,‡; Grissom, Thomas E.∗,†,‡; Betzold, Richard D.†,‡; Scalea, Thomas M.†,‡; Kozar, Rosemary A.†,‡

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doi: 10.1097/SHK.0000000000001608
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Administration of tranexamic acid (TXA) to patients at risk for hemorrhagic shock is a common practice in prehospital and emergency department settings and is recommended by multiple organizations (1–4). Tranexamic acid is a lysine analog that binds to the plasminogen molecule and prevents the conversion of plasminogen to plasmin, thereby inhibiting the breakdown of fibrin clot (5). The results from the Clinical Randomization of an Antifibrinolytic in Significant Hemorrhage 2 (CRASH-2) trial suggested a survival benefit in patients with suspected hemorrhage who received TXA within 3 h of injury (6). The large-scale impact of this trial generated significant enthusiasm in the management of potentially preventable morbidity and mortality related to hemorrhage following traumatic injury. Tranexamic acid administration has also expanded beyond the trauma population and is frequently encountered in orthopedic surgery (7–10), obstetrics, such as post-partum hemorrhage (11), and large volume blood loss in general surgery (12). However, as our understanding of the complexity of trauma-induced coagulopathy matures, the clinical profile and indications for TXA use in trauma are being critically examined.

Fibrinolysis is a physiologic adaptation to minimize disseminated coagulation and thrombosis during hemorrhage and is mediated in part by the release of tissue plasminogen activator (tPA) via generation by the plasminogen–plasmin system (13). Excessive fibrinolysis, as measured by thromboelastography (TEG), is associated with severe injury, increased blood product utilization, and mortality in trauma patients (14). It is in this population that TXA is hypothesized to exert a significant clinical benefit by inhibiting plasminogen conversion to plasmin (14–17). However, there are a number of studies that do not demonstrate a survival benefit in trauma patients with hyperfibrinolysis who are administered TXA (18–20).

Recently, Moore et al. (21) described three fibrinolysis phenotypes that characterize a potentially broad range of coagulation: fibrinolysis shutdown, physiologic fibrinolysis, and hyperfibrinolysis. Fibrinolysis shutdown is associated with severe tissue injury and pathologically represents initial activation of the fibrinolytic system with subsequent inhibition and dysregulated coagulation that exceeds normal physiologic homeostasis (22). Physiologic fibrinolysis reflects a normal response to injury and coagulation such that regulated fibrin clearance minimizes occlusion of the microcirculation, while hyperfibrinolysis is often the extreme result of hemorrhagic shock, profound ischemia, and systemic hypoperfusion (13). There appear to exist differences in mortality, and causes of mortality, among the fibrinolysis phenotypes; however, the association and impact of TXA was not evaluated (21, 23). Therefore, the purpose of this investigation is to evaluate TXA administration and the association with clinical outcomes in a population of severely injured trauma patients and specifically among the fibrinolysis phenotypes. We hypothesize that TXA is associated with increased rates of MOF.


This is a retrospective investigation at a single academic, quaternary care trauma center. Following approval from the Institutional Review Board we searched the institution's trauma registry from a period of October 1, 2015 to October 31, 2017. Inclusion criteria were adult patients age 18 to 89 years, Injury Severity Score (ISS) >16, transferred from the scene of injury, and who had a TEG obtained within 30 min of arrival to the trauma center. Patients who were transferred from an outside facility, sustained a cardiac arrest prior to arrival, had a prior history of taking anticoagulant or antiplatelet medications, or who did not have a TEG obtained within 30 min of presentation, were excluded. We collected baseline patient demographics, injury characteristics, admission vital signs, physiologic data, and International Normalized Ratio (INR) values. It is routine practice at our institution to obtain a TEG on all highest-level trauma activations. All TEG and INR values were obtained within 5 min of each other.

TEG analysis was performed by kaolin-TEG with a TEG 5000 Thromboelastograph Hemostasis Analyzer (Haemonetics, Niles, Ill) via blood collected in 3.2% sodium citrate tubes (BD Vacutainer, 4.5 mL; BD, Franklin Lakes, NJ). The following TEG values were recorded: k-time (minutes), α-angle (degrees), maximum amplitude (MA, mm), and lysis at 30 min (LY30, %). Specific fibrinolysis phenotypes were further defined as follows: Shutdown- LY30 ≤ 0.8%, Physiologic- LY30 0.81% to 2.9%, and Hyperfibrinolysis- LY30 ≥ 3.0%, as is consistent with previous work by Moore et al. (21). Furthermore, administration and timing of TXA was determined by review of intraoperative and medication administration records. The decision to administer TXA was at the discretion of the admitting trauma service or anesthesiologist for patients transferred immediately to the operating room. During the study period, there was no established protocol whereby TXA was administered or withheld based on TEG results. Tranexamic acid was administered intravenously to all included participants. All TEG values were obtained prior to administration of TXA.

Primary outcomes were 28-day mortality and 28-day MOF. The Denver organ failure score was used to determine MOF. This score is well validated in the trauma literature and consists of an evaluation of four organ systems (cardiac, pulmonary, hepatic, and renal) on each day of intensive care unit (ICU) stay (24). The organ failure score for each system was calculated daily on a scale of 0 to 3, with the summation of scores for the four organ systems comprising the total organ failure score. MOF was considered if the total daily sum of the worst scores from each organ system was >3, with the first event of MOF occurring at least 48 h after admission to the ICU. Secondary outcomes were transfused units of packed red blood cells (PRBCs) in the first 3 h and 24 h after hospital admission.

Descriptive statistics were performed on the entire study population. Univariate analysis was utilized to evaluate demographic, injury characteristics, physiologic markers, and fibrinolysis phenotypes as the independent variable and mortality and MOF as the dependent variables. Linear variables were evaluated with the Kruskal–Wallis test and are presented as the median and interquartile range (IQR). Categorial variables were assessed with chi-square testing and Fisher exact test, when appropriate, and are presented as frequency and percent (n, %). Furthermore, the association of TXA administration on mortality was tested in each of the fibrinolysis phenotypes. Statistical significance was considered for a P value < 0.05. A Bonferroni correction was applied for instances of multiple testing for the outcomes of mortality and MOF. Therefore, for these outcomes a P value < 0.016 was considered statistically significant.

A multivariable logistic regression model evaluated the risk of MOF in patients who received TXA, after adjusting for confounding variables. The selection of variables was conducted via forward stepwise selection of statistically significant variables from univariate analysis. Odds ratios (ORs) are reported with 95% confidence intervals (CI). Collinearity was evaluated by the variance inflation factor. Model calibration was tested with the Pearson chi-square goodness-of-fit test and model discrimination was evaluated with the area under the receiver operator characteristic (AUROC) curve. Due to the small number of outcomes events among each of the fibrinolysis phenotypes, multivariable logistic regression modeling was not performed by specific phenotype. All statistical analyses were performed with Stata software version 12.1 (Stata Corp, College Station, Tex). As there is no primary outcome data to suggest MOF rates in patients with fibrinolysis who received TXA, an a priori sample size calculation was not performed. Therefore, results should be interpreted as exploratory in nature.


Four hundred twenty patients were available for final study analysis. A majority of patients were male (335/420, 79.8%), of white race (227/420, 54.0%), and sustained blunt trauma (300/420, 71.5%). The median age was 37 (IQR: 26–55) years and the median ISS was 26 (IQR: 21–33). Median time to TEG was 10.8 (IQR: 7.8–15.0) min. Of the entire study population, 28-day mortality was 60/420 (14.3%) and 28-day MOF occurred in 27/420 (6.4%) patients. Median time to death was 2.9 (IQR: 1.3–6.8) days and median time to MOF was 4 (IQR: 3–7) days.

Fibrinolysis shutdown was observed in 144 of 420 (34.2%) patients, physiologic fibrinolysis in 96 of 420 (22.9%), and hyperfibrinolysis in 180 of 420 (42.9%). There was no difference in ISS by phenotype (Shutdown: 26, IQR: 22–30 vs Physiologic: 25, IQR 19–33 vs Hyperfibrinolysis: 26, IQR 21–33; P = 0.74). There was no significant difference with 28-day mortality by fibrinolysis phenotype (Shutdown: 23/144, 16.0% vs Physiologic: 12/96, 12.5% vs Hyperfibrinolysis: 25/180, 14.0%; P = 0.74) or MOF (Shutdown: 8/144, 5.6% vs Physiologic: 8/96, 8.3% vs Hyperfibrinolysis: 12/180, 6.7%; P = 0.70).

Tranexamic acid was administered to 46/420 (11.0%) patients (Fibrinolysis shutdown: 11/144, 7.6%; Physiologic fibrinolysis: 5/96, 5.2%; Hyperfibrinolysis: 30/180, 16.7%; P = 0.001). Median time to TXA administration was 1.78 (IQR: 0.66–3.33) h after admission. Eleven patients (23.9%) received TXA >3 h after admission and none of the patients died. Of the entire population that was administered TXA, two patients received a bolus of 2 g; all other patients received a 1-g bolus. Fifteen patients (32.6%) received a 1-g infusion following the initial TXA bolus. There was no difference in mortality or MOF among patients who were administered a TXA infusion compared to those who were not (P>0.05). Patients who received TXA had greater ISS (30.0, IQR: 22.0–39.5 vs 26, IQR: 20.5–30.0; P = 0.003), lower admission SBP (122.5, IQR: 94.5–136.5 vs 135, IQR: 119–157; P < 0.001), greater lactate (8.2, IQR: 5.2–12.5 vs 3.6, IQR: 2.7–5.2; P < 0.001), increased INR (1.3, IQR: 1.2–1.6 vs 1.1, IQR: 1.0–1.2; P < 0.001), and lower fibrinogen (193, IQR: 152.5–230.5 vs 258, IQR: 213–311; P < 0.001).

Among the entire study population, there was no difference in mortality between patients who received TXA compared to those who did not receive TXA (8/46, 17.4% vs 52/374, 13.9%; P = 0.52). However, there was a significant increase in MOF in patients who received TXA (8/46, 23.9% vs 16/374, 4.3%; P < 0.001). Patients who developed MOF were more severely injured by ISS (33, IQR: 26–41 vs 26, IQR: 21–30; P = 0.001), had a greater depth of shock by admission lactate (6.5, IQR: 3.6–10.5 vs 3.7, IQR: 2.7–5.6; P < 0.001), and had higher admission INR (1.3, IQR: 1.2–1.6 vs 1.1, IQR: 1.0–1.2; P < 0.001) compared to patients without MOF. A multivariable logistic regression model demonstrated that TXA was associated with an increased risk of MOF (OR: 3.2, 95% CI 1.2–8.9), after adjusting for ISS (1.0, 95% CI 1.0–1.1), admission lactate (OR: 1.1, 95% CI 1.0–1.20), and admission INR (OR: 1.6, 95% CI 0.8–3.3). There was no evidence to suggest lack of model fit by the goodness of fit test (P > 0.05), and the AUROC for the model was 0.82. There was no multicollinearity among variables in the model.

Each fibrinolysis phenotype group was evaluated with respect to TXA and the characteristics of each group are described in Tables 1 and 2, and Table 3 for fibrinolysis shutdown, physiologic fibrinolysis, and hyperfibrinolysis, respectively. There was no difference in mortality among patients who received TXA in any of the fibrinolysis phenotypes (Table 4). However, patients who received TXA in the fibrinolysis shutdown phenotype were significantly more likely to have MOF (3/12, 25.0% vs 6/133, 4.5%; P = 0.005). Similar observations were made for patients in the hyperfibrinolysis group that received TXA (7/30, 23.3% vs 5/150, 3.3%; P = 0.001). There was no difference in MOF among patients who received TXA in the physiologic phenotype (Table 5).

Table 1 - Fibrinolysis shutdown
TXA No-TXA P value
Age, median (IQR) 38.5 (25.0–52.5) 45.0 (27.0–63.0) 0.38
ISS, median (IQR) 29 (22–41) 26 (21–30) 0.10
Lactate, median (IQR) 5.7 (4.3–6.5) 3.4 (2.4–4.5) 0.002
SBP, mm Hg, median (IQR) 120 (92–126) 137 (121–161) 0.001
INR, median (IQR) 1.2 (1.2–1.4) 1.1 (1.0–1.2) 0.03
R-time, median (IQR) 3.3 (2.8–3.8) 3.2 (2.5–3.7) 0.63
K-time, median (IQR) 1.3 (1.1–1.6) 1.3 (1.1–1.6) 0.65
α-angle, median (IQR) 71.0 (67.2–74.4) 71.6 (67.2–74.5) 0.98
MA, median (IQR) 64.9 (59.6–66.1) 64.9 (60.1–69.0) 0.74
LY30, median (IQR) 0 (0.0–0.3) 0.2 (0.0–0.4) 0.20
INR indicates international normalized ratio; IQR, interquartile range; ISS, injury severity score; LY30, % lysis at 30 min; MA, maximum amplitude; SBP, systolic blood pressure; TXA, tranexamic acid.

Table 2 - Physiologic fibrinolysis
TXA No-TXA P value
Age, median (IQR) 49.5 (47.0–63.0) 34.5 (26.0–53.0) 0.10
ISS, median (IQR) 24 (21–30) 25 (19–33) 0.75
Lactate, median (IQR) 3.2 (2.8–3.8) 3.3 (2.3–4.9) 0.67
SBP, mm Hg, median (IQR) 138 (138–146) 134 (123–152) 0.57
INR, median (IQR) 1.1 (1.0–1.2) 1.1 (1.0–1.2) 0.82
R-time, median (IQR) 2.8 (2.7–2.8) 3.2 (2.6–3.8) 0.14
K-time, median (IQR) 1.1 (0.8–1.2) 1.2 (1.0–1.4) 0.22
α-angle, median (IQR) 74.2 (73.6–77.3) 72.2 (70.1–75.4) 0.14
MA, median (IQR) 65.7 (65.1–71.1) 65.3 (61.0–68.1) 0.33
LY30, median (IQR) 1.4 (1.2–1.7) 1.6 (1.2–2.2) 0.67
INR indicates international normalized ratio; IQR, interquartile range; ISS, injury severity score; LY30, % lysis at 30 min; MA, maximum amplitude; SBP, systolic blood pressure; TXA, tranexamic acid.

Table 3 - Hyperfibrinolysis
TXA No-TXA P value
Age, median (IQR) 33.0 (25.0–48.0) 34.0 (26.0–49.0) 0.50
ISS, median (IQR) 30 (26–38) 26 (20–30) 0.006
Lactate, median (IQR) 11.2 (7.9–14.4) 4.2 (2.9–6.3) 0.001
SBP, mm Hg, median (IQR) 115.5 (88.0–131.0) 132.2 (112.0–156.0) 0.001
INR, median (IQR) 1.4 (1.3–1.8) 1.1 (1.0–1.2) 0.001
R-time, median (IQR) 3.2 (2.9–3.8) 3.2 (2.9–3.8) 0.63
K-time, median (IQR) 1.5 (1.2–1.9) 1.2 (1.0–1.4) 0.004
α-angle, median (IQR) 70.0 (62.7–74.0) 72.4 (69.4–75.5) 0.02
MA, median (IQR) 55.1 (46.8–61.2) 60.9 (56.5–65.4) 0.002
LY30, median (IQR) 11.0 (5.7–30.1) 5.9 (3.8–12.7) 0.002
INR indicates international normalized ratio; IQR, interquartile range; ISS, injury severity score; LY30, % lysis at 30 min; MA, maximum amplitude; SBP, systolic blood pressure; TXA, tranexamic acid.

Table 4 - Tranexamic acid and mortality by fibrinolysis phenotypes
TXA No-TXA P value
Shutdown, n (%) 1/11 (9.1) 22/133 (16.5) 0.52
Physiologic, n (%) 0/5 (0) 12/91 (13.2) 0.39
Hyperfibrinolysis, n (%) 7/30 (23.3) 18/150 (12.0) 0.10
TXA indicates tranexamic acid.

Table 5 - Tranexamic acid and multiple organ failure by fibrinolysis phenotypes
TXA No-TXA P value
Shutdown, n (%) 3/11 (27.3) 5/133 (3.8) 0.001
Physiologic, n (%) 1/5 (20.0) 7/91 (7.7) 0.33
Hyperfibrinolysis, n (%) 7/30 (23.3) 5/150 (3.3) 0.001
TXA indicates tranexamic acid.

Tranexamic acid administration was associated with increased units of PRBC transfusion at 3 h (8.5, IQR: 3.5–14.5 vs 0, IQR: 0–2; P < 0.001) and 24 h (12, IQR: 5–30 vs 0, IQR: 0–4; P < 0.001). Furthermore, patients who received TXA in the fibrinolysis shutdown and hyperfibrinolysis groups received significantly more PRBCs (Table 6). There was no significant difference in PRBCs at any time point in the physiologic fibrinolysis patients who were administered TXA (Table 6).

Table 6 - Red blood cell transfusion by TXA and fibrinolysis phenotype
TXA No-TXA P value
 3 h PRBC, md (IQR) 5 (2–15) 0 (0–2) <0.001
 24 h PRBC, md (IQR) 10 (5–37) 0 (0–3) <0.001
 3 h PRBC, md (IQR) 0 (0–4) 0 (0–0) 0.42
 24 h PRBC, md (IQR) 1 (0–4) 0 (0–2) 0.34
 3 h PRBC, md (IQR) 10 (6–14) 0 (0–4) <0.001
 24 h PRBC, md (IQR) 15 (6–33) 1 (0–5) <0.001
IQR indicates interquartile range; md, median; PRBC, packed red blood cell; TXA, tranexamic acid.


Post-traumatic hemorrhage and coagulopathy remain one of the leading causes of death and disability following traumatic injury. The results from the CRASH-2 trial demonstrated significantly lower mortality in patients suspected to be bleeding who received TXA (6). The recent publication of the CRASH-3 trial has also invigorated widespread use of TXA in patients with traumatic brain injury (25). However, numerous limitations, methodologic questions, and the overall applicability of these studies in a mature trauma system raise questions to the universal administration of TXA to all trauma patients. Subsequent investigations have failed to demonstrate a benefit in mortality when TXA is administered to patients with hyperfibrinolysis (18, 19). Moore et al. demonstrated a U-shaped mortality curve among the different phenotypes of fibrinolysis (i.e., fibrinolysis shutdown, physiologic fibrinolysis, and hyperfibrinolysis) such that fibrinolysis shutdown and hyperfibrinolysis are associated with increased mortality following traumatic injury (21, 23). The most frequent cause of death in their study in the fibrinolysis shutdown phenotype was related to MOF. More recent single-center evidence from the United States demonstrates a greater incidence of thrombotic events in patients administered TXA after severe traumatic injury compared to what was reported in the CRASH-2 trial (26). This is significant because a majority of patients received only a single bolus dose of TXA within 3 h of injury. Multiple prospective trials are awaiting publication of results investigating the impact of large, single-dose administration of TXA administration in trauma patients (27, 28). Therefore, it is becoming increasingly necessary to further explore the potential adverse complications following TXA administration.

We observed in patients who received TXA a significant difference in rates of MOF. This is consistent with that reported by Khan et al. (18) which reported MOF as a secondary outcome in patients with hyperfibrinolysis that received TXA. In the present investigation, the risk of MOF remained significant, after adjusting for injury severity, coagulopathy, and depth of shock as measured by serum lactate. However, it is critically important to acknowledge that we cannot prove, nor does the data suggest, that TXA was the cause of increased MOF. Our findings may likely be explained by the fact that patients who were administered TXA were more severely injured and with worse coagulopathy. Despite no collinearity with ISS, INR, lactate, and TXA in the multivariable model, the significantly greater odds ratio for MOF in the patients who received TXA may simply reflect a marker of “sicker” patients that the aforementioned variables were unable to identify. This has also been identified in previous findings by Harvin et al. (19) and Cole et al. (29). Patients in the fibrinolysis shutdown and hyperfibrinolysis phenotypes, as well as those who received TXA, received greater amounts of blood transfusion. This is consistent with prior observations (19, 29, 30). Nonetheless, this data further demonstrates the likely underlying complexity involved with TXA, coagulation, and post-traumatic fibrinolysis. Previous investigations report different rates of admission coagulopathy, as measured by INR, in patients with hyperfibrinolysis who received TXA (18, 19). Even among the fibrinolysis phenotypes there are likely intrinsic differences in underlying post-traumatic coagulation (31–33).

The results of our investigation also identified that TXA administration to trauma patients with fibrinolysis shutdown was associated with increased MOF. The overall number of outcome events in patients who received TXA was rather small (n = 3) and it is important to acknowledge that this observation from our data is strictly an association and does not prove causation. However, there are numerous recent discussions in the trauma literature regarding certain cellular-based mechanisms in the fibrinolysis phenotypes (22). It is possible that the fibrinolysis shutdown phenotype is associated with severe tissue injury that predisposes to microvascular fibrin deposition, thrombus formation and subsequent tissue ischemia and organ dysfunction (34). PAI-1 levels are associated with MOF in trauma patients who developed disseminated intravascular coagulopathy (35). Therefore, it is hypothesized that the interaction of TXA in patients with fibrinolysis shutdown may result in excessive accumulation of fibrin deposits contributing to organ dysfunction (36, 37). It is also plausible that in the fibrinolysis shutdown phenotype the response to severe injury results in an impaired regulation of fibrinolysis, such as reduced sensitivity to tPA (33, 38). Furthermore, emerging discussions recognize potentially multiple phenotypic forms of fibrinolysis shutdown and hyperfibrinolysis, such that fibrinolysis is dramatically more intricate and complex (22). Our data is unable to prove these mechanisms and therefore these explanations are strictly hypothesis generating.

There are limitations to the present investigation. This was a retrospective study from a single, academic trauma center and contains inherent bias. As previously discussed, our results can only demonstrate an association with TXA and MOF and this does not imply causation. The number of outcome events in the fibrinolysis phenotypes was small and precluded multivariable logistic regression modeling and controlling for potential confounding variables in each of the individual phenotypes. We included adult patients, transferred from the scene of injury, and with an ISS > 16. Therefore, these results are not necessarily applicable to all trauma patients. The distribution of fibrinolysis phenotypes is different from prior studies; we identified a higher incidence of hyperfibrinolysis in our cohort than has been described in previous investigations. This may reflect characteristics of patient and trauma center population. There was also a low rate of TXA administration (∼10% of the overall cohort and 17% of patients with hyperfibrinolysis). This is lower than that which was reported by Khan et al. (18) but similar to prior work from Meizoso et al. (39) and Harvin et al. (19). We were unable to obtain volumes of prehospital crystalloid that were administered and the impact this may have on admission coagulopathy. However, it would be rare that patients receive any significant volume of crystalloids prior to arrival. Last, in patients who received TXA nearly one-quarter were administered the drug 3 h after admission. While we observed no differences in mortality or MOF in patients who received TXA beyond 3 h, this is in contradiction to certain guidelines (4).

The potential clinical implications of this study contribute further information to the growing interest in TXA (12, 13, 38). While early TXA administration is advocated by a number of professional organizations as a method to minimize hemorrhage (8, 11) and reduce mortality (1), recent statements advocate a more nuanced and sophisticated approach is necessary (13, 22, 38, 40). It is becoming more apparent that even among fibrinolysis phenotypes there are significant differences in post-traumatic coagulopathy (22, 31–33). These differences must be critically investigated to further understand fibrinolysis and the role of TXA in the cellular-based dynamics of acute traumatic coagulopathy and resuscitation after traumatic injury. While the potential benefit of early TXA administration is supported by prospective, randomized trials (6, 25), it is also possible that the contribution of TXA may be dependent upon other measures of resuscitation that address the post-traumatic coagulopathy (41, 42). It is important to acknowledge that the purpose of this investigation is not to suggest TXA be eliminated from the resuscitation of trauma patients. Rather our data provides further evidence to the growing discussion on TXA in the trauma population that seeks to address the complex interaction of injury severity, fibrinolysis, coagulopathy, resuscitation, and the clinical outcomes of mortality and MOF. Furthermore, we also acknowledge that beneficial mechanisms of TXA may not be completely understood and extend beyond fibrinolysis and coagulation (43, 44).


Post-traumatic fibrinolysis is emerging as a complex phenomenon in severely injured patients. We found that administration of TXA was associated with an increased risk of MOF, after adjusting for ISS, admission lactate, and INR. Specifically, there was a significant increase in MOF among patients who received TXA in the fibrinolysis shutdown and hyperfibrinolysis groups, but not the physiologic phenotype. These observations do not prove causation and therefore further scientific evaluation with large, multicenter studies is necessary to further define the impact of TXA in the resuscitation of severely injured trauma patients.


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Fibrinolysis; mortality; multiple organ failure; tranexamic acid

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